Ibuprofen is a nonsteroidal anti-inflammatory agent (NSAIA) or nonsteroidal anti-inflammatory drug (NSAID), with analgesic and antipyretic properties. Ibuprofen has pharmacologic actions similar to those of other prototypical NSAIAs, which are thought to act through inhibition of prostaglandin synthesis. It’s used temporarily relieves minor aches and pains due to: headache; the common cold; muscular aches; backache; toothache; minor pain of arthritis; menstrual cramps and temporarily reduces fever. The exact mechanism of action of ibuprofen is unknown. Ibuprofen is a non-selective inhibitor of cyclooxygenase, an enzyme invovled in prostaglandin synthesis via the arachidonic acid pathway. Its pharmacological effects are believed to be due to inhibition cylooxygenase-2 (COX-2) which decreases the synthesis of prostaglandins involved in mediating inflammation, pain, fever and swelling. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. Inhibition of COX-1 is thought to cause some of the side effects of ibuprofen including GI ulceration. Ibuprofen is administered as a racemic mixture. The R-enantiomer undergoes extensive interconversion to the S-enantiomer in vivo. The S-enantiomer is believed to be the more pharmacologically active enantiomer.

(R)-Ibuprofen, a nonsteroidal anti-inflammatory, is the less active enantiomer of ibuprofen. (S)-enantiomer of ibuprofen has the desired therapeutic effect (160 times more active than its (R)-enantiomer) in the in vitro inhibition of prostaglandin synthesis, while the (R)- ibuprofen is inactive. The accumulation of (R)- ibuprofen can cause serious side effects to the human body such as gastrointestinal pain and production of “hybrid” triglycerides between (R)- ibuprofen and Coenzyme A, which disrupt normal lipid metabolism and membrane function. The R(-)-isomer is almost inactive in inhibiting COX-2.